# Posterior Vitreous Detachment and Vitreous Hemorrhage

## Posterior Vitreous Detachment (PVD)

### Vitreous Anatomy

The vitreous humor is a transparent gel that fills the posterior 80% of the globe, occupying a volume of approximately 4 mL. It is composed of 99% water and 1% structural components, primarily type II collagen fibrils and hyaluronic acid. The vitreous is not uniformly adherent to the retina -- its attachments vary in strength at different locations. The vitreous base, which straddles the ora serrata extending 2 mm anteriorly and 3 mm posteriorly, is the strongest attachment and never detaches spontaneously. Other sites of firm adhesion include the optic disc margin, the fovea, along retinal vessels, and at the borders of lattice degeneration. The vitreous cortex is a dense peripheral layer that lies directly adherent to the internal limiting membrane of the retina.

### Pathophysiology

With aging, the vitreous undergoes liquefaction -- a process called synchysis -- in which collagen fibrils aggregate and clump together, creating lacunae of liquid vitreous within the gel. Simultaneously, the adhesion between the vitreous cortex and the internal limiting membrane weakens. Eventually, the vitreous cortex separates from the ILM, producing a posterior vitreous detachment. This separation typically begins in the perifoveal region and progresses anteriorly toward the optic disc and the vitreous base. When the vitreous separates from the optic disc margin, it releases an annular condensation of prepapillary glial tissue known as a Weiss ring, which is visible to the patient as a prominent new floater.

### Epidemiology

PVD most commonly presents in patients between the ages of 50 and 75. Certain conditions promote earlier onset, including myopia, prior cataract surgery, ocular trauma, intraocular inflammation, and diabetic vitreopathy. By the age of 80, PVD is present in more than 80% of eyes.

### Clinical Presentation

Patients typically present with sudden-onset floaters, which may take the form of a ring-shaped opacity (the Weiss ring) or cobweb-like strands. Photopsia -- brief flashes of light, usually perceived in the temporal visual field -- results from mechanical stimulation of the retina by vitreous traction. Although the symptoms are acute and often alarming, most PVDs are benign and self-limited. The critical clinical task is to distinguish an uncomplicated PVD from one complicated by a retinal break or detachment.

### Complications of Acute PVD

Eight to fifteen percent of symptomatic PVDs are associated with a retinal tear. Vitreous hemorrhage may occur when a retinal vessel is torn during the separation process, obscuring the fundus view. If a retinal break is not identified and treated, it may progress to a rhegmatogenous retinal detachment. The risk of retinal tear is highest during the first six weeks after symptom onset.

### Examination

A thorough dilated fundoscopy with scleral depression of the entire retinal periphery is essential. The Shafer sign -- pigmented cells (tobacco dust) visible in the anterior vitreous -- is pathognomonic for a retinal break and must be actively sought on slit-lamp examination. When vitreous hemorrhage or other media opacity prevents adequate fundoscopy, B-scan ultrasonography is mandatory to rule out retinal detachment and assess PVD status. OCT can confirm the presence of PVD, though the clinical examination remains the primary diagnostic tool.

### Follow-Up Protocol for Acute Symptomatic PVD

If no retinal tear is found at the initial examination, the patient should be re-examined in four to six weeks, as retinal tears can develop after the initial evaluation. Any new symptoms -- increased floaters, new flashes, or a visual field defect -- should trigger urgent re-evaluation. When a retinal tear is identified, prophylactic laser retinopexy or cryopexy should be performed within 24 to 72 hours. If vitreous hemorrhage is present without a visible retinal break, close follow-up with serial B-scan ultrasonography is indicated, and pars plana vitrectomy should be considered if the hemorrhage does not clear.

<image>B-scan ultrasound showing complete posterior vitreous detachment with the posterior hyaloid face separated from the retinal surface and attached at the optic disc, with Weiss ring visible</image>

## Vitreous Hemorrhage

### Definition

Vitreous hemorrhage refers to the presence of blood within the vitreous cavity, which may be located within the vitreous gel itself (intragel), in the subhyaloid or preretinal space, or in the retrohyaloid space between the detached posterior hyaloid face and the retinal surface.

### Etiology (Differential Diagnosis)

The most common causes of vitreous hemorrhage in adults are proliferative diabetic retinopathy, which accounts for 30 to 40% of cases overall, posterior vitreous detachment with an associated retinal tear (15 to 30%), and retinal vein occlusion with secondary neovascularization. Other important causes include trauma (including non-accidental injury in children), sickle cell retinopathy, retinal macroaneurysm, breakthrough hemorrhage from choroidal neovascularization in age-related macular degeneration, Terson syndrome (vitreous hemorrhage associated with subarachnoid hemorrhage), blood dyscrasias or anticoagulation, retinal vasculitis, Valsalva retinopathy (which produces a characteristic preretinal hemorrhage), and intraocular tumors such as choroidal melanoma and retinoblastoma.

| Cause | Frequency | Key Clinical Clue | Urgency |
|---|---|---|---|
| Proliferative diabetic retinopathy | 30-40% | Known diabetes; NVI; fellow eye PDR | High -- anti-VEGF +/- vitrectomy |
| PVD with retinal tear | 15-30% | Acute floaters/flashes; Shafer sign | Urgent -- laser/cryo within 24-72 hrs |
| Retinal vein occlusion | 10-15% | Dilated tortuous veins; known RVO | High -- treat underlying cause |
| Trauma | Variable | History of injury; rule out open globe | Emergent if open globe |
| Sickle cell retinopathy | Variable | Young patient; known sickle cell | Moderate |
| Retinal macroaneurysm | 5% | Hypertensive elderly; focal aneurysm | Moderate |
| Terson syndrome | Rare | Acute subarachnoid hemorrhage | Neurosurgical emergency |
| Intraocular tumor | Rare | Mass on B-scan; retinoblastoma in children | High -- oncology referral |

### Clinical Presentation

Vitreous hemorrhage presents as sudden painless vision loss or an acute increase in floaters. The severity ranges from mild vitreous haze with a few blood cells to dense hemorrhage that completely obscures the fundus view. The red reflex may be absent in severe cases. Blood may layer inferiorly due to gravitational settling.

### Evaluation

A detailed history should address diabetes, trauma, anticoagulant use, sickle cell disease, and prior ocular surgery. The examination includes visual acuity assessment, intraocular pressure measurement, slit-lamp examination with specific attention to the iris for neovascularization, and a dilated fundus examination when possible. B-scan ultrasonography is essential when the fundus view is obscured, as it can rule out retinal detachment, assess PVD status, identify an intraocular mass, and grade hemorrhage severity. The fellow eye should always be examined, as it may reveal the underlying diagnosis -- for example, proliferative diabetic retinopathy changes or findings consistent with a retinal vein occlusion. Systemic workup is guided by the suspected etiology and may include glucose, hemoglobin A1c, complete blood count, coagulation studies, and sickle cell screening.

<image>Clinical photograph demonstrating dense vitreous hemorrhage obscuring the fundus view with corresponding B-scan ultrasound confirming attached retina and posterior vitreous detachment</image>

### Management

#### Conservative/Observation

Mild vitreous hemorrhage with a known benign etiology, such as a PVD without an associated retinal tear, can be observed. The head of the bed should be elevated to allow blood to settle inferiorly and clear the visual axis. Anticoagulants should be avoided if clinically feasible, in coordination with the patient's primary care team. Serial B-scan ultrasonography should be performed to monitor for retinal detachment, and visual acuity recovery should be followed.

#### Urgent Intervention Needed

Urgent surgical intervention is required when B-scan ultrasonography detects a retinal detachment, when a retinal tear is known or suspected, in cases of open globe injury, when endophthalmitis is present, and for ghost cell glaucoma.

#### Vitrectomy Indications

Pars plana vitrectomy is indicated for non-clearing vitreous hemorrhage. In type 1 diabetic patients, early vitrectomy within one month should be considered based on the Diabetic Retinopathy Vitrectomy Study findings. In type 2 diabetic patients without detachment, observation for one to three months is reasonable before proceeding to surgery. Other indications include vitreous hemorrhage associated with retinal detachment, dense hemorrhage preventing adequate panretinal photocoagulation in PDR with active neovascularization, ghost cell or hemolytic glaucoma, and functional visual impairment in a monocular patient.

#### Special Considerations by Etiology

In proliferative diabetic retinopathy, anti-VEGF injection can be administered even through dense vitreous hemorrhage, as it helps reduce neovascularization and may accelerate hemorrhage clearance; PRP should be applied as soon as the view permits. For PVD-associated hemorrhage, laser or cryopexy should be applied to any visible retinal break, and vitrectomy considered if the break cannot be identified and the hemorrhage does not clear. In retinal vein occlusion, the underlying cause must be treated and anti-VEGF administered for neovascularization. In traumatic vitreous hemorrhage, an open globe must be ruled out, and vitrectomy is indicated for non-clearing hemorrhage or associated retinal detachment.

## Ghost Cell Glaucoma

Ghost cell glaucoma is a secondary open-angle glaucoma that occurs weeks to months after vitreous hemorrhage. The pathophysiology involves degeneration of red blood cells within the vitreous cavity: these ghost cells lose their hemoglobin, become rigid and khaki-colored, and migrate into the anterior chamber where they obstruct the trabecular meshwork, producing elevated intraocular pressure. Treatment consists of aqueous suppressants for IOP control, with vitrectomy indicated in refractory cases to remove the source of ghost cells.

<image>Slit-lamp photograph showing ghost cells (khaki-colored degenerated erythrocytes) in the anterior chamber of a patient with ghost cell glaucoma following vitreous hemorrhage</image>

## Clinical Pearls

Every patient presenting with an acute PVD and symptoms of flashes or floaters deserves a thorough dilated examination with scleral depression of the entire retinal periphery, as the risk of an associated retinal tear is approximately 10%. The Shafer sign is the single most reliable indicator of a retinal break; a clear anterior vitreous is reassuring but does not eliminate the need for a careful peripheral examination. When dense vitreous hemorrhage prevents adequate fundoscopy, B-scan ultrasonography is mandatory to rule out retinal detachment. The most common cause of vitreous hemorrhage varies by population: proliferative diabetic retinopathy predominates in diabetic patients, while PVD-related retinal tears are the leading cause in the non-diabetic elderly. The fellow eye should always be examined, as it often provides diagnostic clues that the affected eye cannot. Terson syndrome -- bilateral vitreous hemorrhage in the setting of acute subarachnoid hemorrhage -- carries a poor neurological prognosis and should prompt urgent neurosurgical evaluation. Anti-VEGF agents can be safely administered through dense vitreous hemorrhage in patients with PDR, even when the retina cannot be visualized. Even when the initial examination after an acute PVD is completely normal, a follow-up examination should be scheduled in four to six weeks, as late retinal breaks do occur.

## References

- Byer NE. Natural history of posterior vitreous detachment with early management as the premier line of defense against retinal detachment. Ophthalmology. 1994;101(9):1503-1514.
- Diabetic Retinopathy Vitrectomy Study Research Group. Early vitrectomy for severe vitreous hemorrhage in diabetic retinopathy (DRVS Report 2). Arch Ophthalmol. 1985;103(11):1644-1652.
- Spraul CW, Grossniklaus HE. Vitreous hemorrhage. Surv Ophthalmol. 1997;42(1):3-39.
- American Academy of Ophthalmology. Basic and Clinical Science Course, Section 12: Retina and Vitreous.